Hypoxia-ischemia is responsible for a high morbidity and mortality rate, both in infant and adult patients. In humans, the brain is immature from fetal to postnatal life, demonstrating more specific vulnerability than the adult one, induced by exposure at perinatal asphyxia. The extension and distribution of brain lesions depend to a large extent on the intensity and exposure to injury, the maturational stage, the affected brain region and the survival time of the patient. Different cellular events are developed in response to hypoxic-ischemic injury. These events have been related to the excitotoxicity (activation of glutamate receptors), energy failure (decrease in ATP levels), inflammatory cascade (delivery of inflammatory mediators), and gene and transcriptional activation.